174) Results obtained showed that aberrant methylation of p15 and p16 genes were detected in 64.29 and 50% of ovarian cancer patients, while E-cadherin hypermethylation was detected in 78.57% of ovarian cancer patients. |
PMID:23572389 DOI:10.1177/0748233713484657 |
2015 Toxicology and industrial health |
* Hypermethylation of P15, P16, and E-cadherin genes in ovarian cancer. |
- Both p16 and p15 proteins are inhibitors of cyclin-dependent kinases that prevent the cell going through the G1/S phase transaction. E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent interactions between adjacent epithelial cells. Two groups of patients were selected: the first group suffered from epithelial serous ovarian tumors and the second group suffered from benign ovarian lesions; ovarian tissue samples from all the subjects (benign and malignant) were subjected to methylation-specific polymerase chain reaction for methylated and unmethylated alleles of the genes (E-cadherin, p15, and p16). Results obtained showed that aberrant methylation of p15 and p16 genes were detected in 64.29 and 50% of ovarian cancer patients, while E-cadherin hypermethylation was detected in 78.57% of ovarian cancer patients. Methylation of E-cadherin was significantly correlated with different stage of disease (p < 0.05). It was found that the risk of E-cadherin hypermethylation was 1.347-fold, while risk of p15 hypermethylation was 1.543-fold and p16 was 1.2-fold among patients with ovarian cancer than that among patients with benign ovarian lesions. In conclusion, Dysfunction of the cell cycle and/or the cell-cell adhesion molecule plays a role in the pathogenesis of ovarian cancer and that the analysis of the methylation of p15 and E-cadherin genes can provide clinically important evidence on which to base the treatment. |
(1)101 and | (12)8 including | (23)4 for | (34)2 13 |
(2)36 *null* | (13)7 encoding | (24)4 from | (35)2 but |
(3)28 are | (14)7 involved | (25)4 related | (36)2 can |
(4)26 were | (15)7 which | (26)4 with | (37)2 coding |
(5)25 in | (16)6 (PCGs), | (27)3 had | (38)2 expressed |
(6)16 2 | (17)6 use | (28)3 have | (39)2 is |
(7)14 (13 | (18)5 may | (29)3 stop | (40)2 on |
(8)14 22 | (19)5 that | (30)3 such | (41)2 ranged |
(9)12 start | (20)4 (PCGs) | (31)2 (cytb, | (42)2 to |
(10)11 of | (21)4 as | (32)2 (pnad1 | |
(11)9 was | (22)4 associated | (33)2 (srfAA, |
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